Differential Effects of 'Vaping' on Lipid and Glucose Profiles and Liver Metabolic Markers in Obese Versus Non-obese Mice

Abstract

Tobacco smoking increases the risk of metabolic disorders due to the combination of harmful chemicals, whereas pure nicotine can improve glucose tolerance. E-cigarette vapour contains nicotine and some of the harmful chemicals found in cigarette smoke at lower levels. To investigate how e-vapour affects metabolic profiles, male Balb/c mice were exposed to a high-fat diet (HFD, 43% fat, 20kJ/g) for 16weeks, and e-vapour in the last 6weeks. HFD alone doubled fat mass and caused dyslipidaemia and glucose intolerance. E-vapour reduced fat mass in HFD-fed mice; only nicotine-containing e-vapour improved glucose tolerance. In chow-fed mice, e-vapour increased lipid content in both blood and liver. Changes in liver metabolic markers may be adaptive responses rather than causal. Future studies can investigate how e-vapour differentially affects metabolic profiles with different diets.

Keywords: abdominal obesity; free fatty acid; glucose tolerance; liver; triglycerides.

Figure 1

Lipid metabolic markers in the liver. Protein level of FASN (A), mRNA expression of ATGL (B) and CPT1a (C) in mice fed a HFD with or without the exposure to e-vapour. The results are expressed as mean±SEM, n=5–8. Data were analysed by two-way ANOVA followed by Fisher’s least significant difference (LSD) post-hoc tests. A conditional t-test for non-overlap of value distributions was performed between the control (Chow+sham or HFD+sham) and interventional groups. ^**p<0.01 diet effect, ^δδp<0.01 e-vapour exposure effect; ^tp<0.05 vs. Chow+Sham by conditional t-test, ^#p<0.05, ^##p<0.01 vs. HFD+Sham, ^†p<0.05 vs. Chow+e-cig18mg and ^‡‡p<0.01 vs. Chow+e-cig0. ATGL, adipose triglyceride lipase; CPT, carnitine palmitoyltransferase; and FASN, fatty acid synthase.

Figure 2

Glucose level during intraperitoneal glucose tolerance test (IPGTT, A) and mRNA expression of markers of inflammation [TNF-α (B), IL-1β (C)], fibrosis (Col1a1, D), insulin sensing (PPARγ, E), glucose transporter [Glut2 (F), Glut4 (G)] and gluconeogenesis [PEPCK (H), FOXO1 (I)] in the liver. The results are expressed as mean±SEM, n=5–8. Data were analysed by two-way ANOVA followed by Fisher’s least significant difference (LSD) post-hoc tests. ^θp<0.05 Chow+e-cig0 vs. HFD+e-cig0; ^ϕp<0.01 Chow+sham vs. HFD+sham; ^φp<0.05 Chow+sham vs. HFD+sham; Chow+e-cig18 vs. HFD+e-cig18; ^*p<0.05, ^**p<0.01 diet effect, ^δp<0.05 e-vapour exposure effect; ^γp<0.05, ^γγp<0.01 vs. Chow+sham; and ^#p<0.05 vs. HFD+Sham, ^†p<0.05; ^††p<0.01 vs. Chow+e-cig18 and ^‡p<0.05 vs. Chow+e-cig0. Col1a1, collagen 1a1; FOXO1, Forkhead box protein O1; Glut, glucose transporter; PEPCK, phosphoenolpyruvate carboxykinase; and PPAR, Peroxisome proliferator-activated receptors.